There is evidence of the connection between extracellular amino acid availability and an antipsychotic’s anticancer efficacy of PIM: the drug blocks lysosomal lipid release, GBM cells compensate by up-regulating the glutamine transporter ASCT2, and co-inhibition of glutamine uptake or GLS (e.g., pimozide + CB-839) collapses this feed-forward loop and markedly enhances tumor suppression [54]. Here, SLC1A5 is linked to glioblastoma.